Planting of potato seed pieces infected with Phytophthora infestans
can lead to the introduction of late blight within a planting. When infected
seed pieces are planted, there are three resulting scenarios: (i) a healthy plant emerges,
(ii) no plant emerges because of the rapid decay of the seed piece, or (iii) a
symptomatic plant emerges. A major factor favoring stand establishment and seed
transmission is the severity of seed piece infection. When infection is severe,
stand is compromised and transmission rate is low. When infection is mild, the
plant emerges before the seed piece decays and, in some instances, the pathogen
makes its way from the seed piece to the plant where a stem lesion is formed. Diseased seed tubers are the principle source of late blight inoculum for
infection of healthy seed pieces. Treatment of infected or blighted seed tubers
with a seed dressing with activity against P. infestans is not a viable
tactic because the products are ineffective against established infections.
Conversely, treatment of healthy seed pieces provides a high level of protection
against late blight spores that are spread during the seed handling and planting
operations. Optimum effectiveness is achieved when products are applied
immediately following cutting, as none are effective against established
infections. Seed treatment reduces the risk of seed transmission of late blight
and enhances stand establishment and plant vigor. This tactic should be an
important component of an integrated late blight management program.

Introduction

Programs to control sources of primary inoculum for late blight epidemics of
potatoes caused by Phytophthora infestans have focused on destruction of
cull piles and management of volunteer potatoes. Although seed tubers are
generally accepted as the principle means by which the pathogen survives from
season to season, their importance as a within-field source of inoculum for
initiating late blight epidemics has often been underestimated.

Within a seed lot, seed pieces will range from noninfected to mildly or
severely diseased depending on the amount of inoculum distributed to the seed
pieces and its ability to infect. For example, when a large amount of inoculum
is deposited on the seed piece, the infection is severe and the seed piece
rapidly succumbs to bacterial soft rot. These seed pieces are not regarded as an
important within-field source of inoculum primarily because they decay before
the sprout has a chance to emerge. On the other hand, a seed piece with a mild
or latent infection will germinate and produce a small or normal-sized plant.
Occasionally, but not commonly, the pathogen makes its way from the seed piece
to the new shoot where the primary symptom is a stem lesion. Generally, the
lesion extends from the seed piece to the above ground stem. In some instances,
however, the above ground lesion is not continuous from the seed piece to the
lower stem. Importantly, most diseased seed pieces do not result in emerging
plants with symptoms of late blight. In fact, seed-to-plant transmission is a
rare event. Soil moisture and temperature, cultivar susceptibility,
physiological age of the seed lot, planting depth, and other factors probably
play a key role in the development of infectious plants grown from seed pieces
infected with P. infestans.

Our research has focused on identifying those factors that favor seed
transmission of P. infestans and compromise stand establishment. Seed
piece treatment as a tactic for protecting seed pieces against spread of the
pathogen during the seed handling operation also has been evaluated. These
studies, done in Oregon and Washington, have included the two predominant
genotypes of the late blight pathogen in the Pacific Northwest, US-8 (A2 mating
type, metalaxyl-insensitive) and US-11 (A1 mating type, metalaxyl-insensitive).

Fig. 2. Transmission of late blight to an emerging sprout from a seed piece
inoculated with sporangia of Phytophthora infestans (click image for larger
view).

Infection. Tubers can become infected with the late blight pathogen in the
field during the growing season, at harvest, and during the seed handling
operation. In the field, spores are washed by rain or irrigation water from
blighted foliage into the soil where they may come in contact with and infect
developing tubers. During the harvesting operation, spores are spread from
diseased vines onto the tuber surface. With both scenarios, the number of spores
landing on and infecting a tuber is quite variable. Some of the tubers will
become severely diseased, some will slowly develop symptoms of blight, and some
will be symptomless, whereas others will remain uninfected. The majority of
severely blighted tubers are short lived because they rot very quickly from
invasion by soft rot bacteria. In contrast, tubers with mild symptoms or latent
infections seldom rot, or they do so slowly. Diseased tubers that survive
storage over winter are the principle source of inoculum for contamination and
subsequent infection of healthy seed pieces. Infection of healthy seed pieces
occurs from spores that are produced on both intact and cut surfaces of blighted
tubers (Fig. 1). Research performed in Maine (10) has shown that on average, one
sporulating seed piece can contaminate and subsequently infect three adjacent,
healthy pieces. If the amount of inoculum deposited on healthy seed pieces is
high, the resulting infection is severe. When these seed pieces are planted, few
germinate because of their rapid decay by the secondary invaders, the soft rot
bacteria. A mild infection results when seed pieces are infected with a small
amount of inoculum (12). The fate of mildly infected seed pieces is two fold: (i)
eyes do not germinate into sprouts because the rapid decay of the seed pieces,
or (ii) plants emerge before the seed piece has a chance to decay completely. Some
of these emerged plants will develop stem lesions of late blight (Fig. 2) within
2 to 5 weeks following emergence. In other plants, stem lesions will not appear
until later in the season (2,7). Regardless of when in the season symptoms
appear, these blighted plants serve as the springboard from which the pathogen is
spread to the surrounding, healthy foliage.

Transmission: Many factors probably influence the rate of seed-transmitted P.
infestans. One factor is pathogen genotype. New immigrant genotypes of P.
infestans, such as US-8 and US-11, are more aggressive on potato tubers than
the previously established US-1 population (9) and have displaced US-1
throughout potato growing areas of the U.S. In a greenhouse study (11) in which
transmission efficiency of US-1 and US-8 was compared, US-1 produced 1.9%
diseased sprouts versus 19.4% with US-8. Another factor is the amount of
inoculum (spores) spread to healthy seed pieces during the seed handling
operation. In general, when seed pieces become contaminated with a large amount
of inoculum, infection is severe (12), and the probability of seed-to-plant
transmission is very low. With a low amount of inoculum, seed piece infection is
mild, and the probability of seed-to-plant transmission is higher. As the sprout
germinates, the pathogen grows into the stem from the seed piece as mycelium
(1,2). When environmental conditions are favorable for disease expression, a
lesion appears on the stem.

Transmission was observed across a range of cultivars with US-8 in western
Oregon and US-11 in western Washington at inoculum densities as low as 2.5, 25,
or 250 spores per seed piece. Transmission frequencies of 0.53% in Oregon and 0.75%
in Washington were recorded in 1999. In our 2000 studies, transmission rates
averaged 2.78% and 1.01% for the respective locations. The time from onset of
emergence until the appearance of stem lesions ranged from 1 to 35 days in
Oregon and 9 to 18 days in western Washington. These observations are in
agreement with studies in New York (3) in the early 1980s with the presumed US-1
genotype where late blight was first observed 17 to 46 days after emergence.

We can estimate the risk of seed transmission from a given seed lot if the
percentage of infected seed pieces is known. If 10% of the seed pieces are
infected and we assume a seed transmission rate of 1.0%, the expected percentage
of blighted seedlings would be 0.1%. At 40,000 plants/ha, there would be
slightly less than 40 incidences of seed transmission/ha. If the seed
transmission rate was 3.0%, the expected percentage of seedlings with late
blight would be 120 incidences/ha. With both scenarios, these are relatively
high rates of seed transmission in a commercial field, given the ability of this
pathogen to rapidly spread from a single infectious plant. The total number of
diseased plants from infected seed pieces in each field, however, is so low that
the problem would likely go undetected prior to secondary spread of the
pathogen.

Stand Establishment: Stand establishment also is impacted by
the number of spores
on the seed piece. For example, with the cultivar Russet Burbank, as the number of
spores per seed piece increased, the severity of seed infection increased. As a
consequence, bacterial seed piece decay increased (Fig. 3) and percent emergence
decreased (Fig. 4). In addition to a reduction in stand in Oregon with US-8, the
onset of emergence was delayed 7 days at the two highest inoculum densities.

Fig. 3. Effect of inoculum density of Phytophthora infestans on
percent seed piece decay of potato cultivar Russet Burbank in Oregon and Washington. Seed pieces were inoculated with sporangia of US-8 in Oregon and US-11 in Washington (click image for larger view).

Fig. 4. Effect of inoculum density of Phytophthora infestans on
emergence of seed pieces of potato cultivar Russet Burbank in Oregon and Washington. Seed pieces were inoculated with sporangia of US-8 in Oregon and US-11 in Washington (click image for larger view).

As with seed transmission, the amount of seed piece decay is mediated by soil
environmental conditions. The ideal soil temperature for planting potatoes is 13
to 15.5°C (14). This temperature encourages quick emergence without promoting the
growth of seed piece decay organisms. Noninoculated seed pieces of cultivar Russet
Burbank achieved 95% emergence 18 and 29 days after planting in Oregon and
Washington, respectively. At the two highest inoculum densities (250 or 2500
sporangia per seed piece), average emergence was 3.3 and 6.7% and 98.1 and 67.3%
for US-8 in Oregon and US-11 in Washington, respectively (Fig. 4) and the
percent seed piece decay for these inoculum densities was 99 and 99% in Oregon
and 21 and 70% in Washington (Fig. 3). This suggests that either US-11 is a less
aggressive pathogen of the seed piece than US-8 or the soil environment was less
conducive for seed piece decay by the soft rot bacteria in Washington.

The Value of Seed Treatment

Products. For management of seedborne diseases, seed treatment is often the
simplest and least costly control measure available. Seed treatments are easily
applied, and the treatments are inexpensive compared to foliar sprays.
Furthermore, plant growth will be more vigorous, and the crop will produce a
greater yield if the seed pieces are free of pathogens.

If spread of late blight during the seed handling operation increases the
risk for seed transmission, then application of a seed dressing is an obvious
preventive approach to managing this phase of the disease. Our research has
shown that a seed piece treatment is effective only when one or more of the
components of the fungicide product has efficacy against P. infestans (6,13). At least four
products containing one or two fungicides (maneb, mancozeb
or cymoxanil plus mancozeb) with activity against P. infestans are
registered. In addition to providing a chemical barrier around healthy seed
pieces, seed treatment also reduces the number of spores produced on the cut
surface of blighted seed pieces, thereby reducing the number of spores that can
be spread during the seed handling operation. All four products were equally
effective in maintaining seed piece health (Fig. 5A and B) and improving
emergence (Fig. 6A and B). When a seed treatment was applied, few seed pieces
decayed (2.4 and 5.6% in Oregon and Washington, respectively), and of those that
did, a bacterial soft rot was the primary cause. Thus, a seed treatment protects
against infection by P. infestans and prevents secondary invasion
by the soft rot bacteria. Typically, products with maneb or mancozeb alone or
mancozeb plus cymoxanil were equally effective in protecting against seedborne P.
infestans. Regardless of product, final emergence approached 100% across a
wide range of inoculum densities (Fig. 7). In contrast, products such as
thiophanate-methyl or fludioxinil, which do not target P. infestans,
do not enhance stand establishment in the presence of the late blight pathogen
and may indirectly allow the transmission of the pathogen from the seed piece to
the sprout (6).

Fig. 5. Effect of potato seed piece treatment on the relationship between
inoculum density of seedborne Phytophthora infestans and percent healthy
seed pieces in (A) Oregon and (B) Washington. Seed pieces of cultivar Shepody were
inoculated with sporangia of US-8 in Oregon and US-11 in Washington and
immediately treated with the seed dressing (click image for larger
view).

Fig. 6. Effect of potato seed piece treatment on the relationship between
inoculum density of seed borne Phytophthora infestans and final emergence
in (A) Oregon and (B) Washington. Seed pieces of cultivar Shepody were inoculated with
sporangia of US-8 in Oregon and US-11 in Washington and immediately treated with
the seed dressing (click image for larger view).

Fig. 7. Field view of trial on efficacy of seed piece treatments for control
of seedborne late blight of potatoes (click image for larger
view).

Timing. The tried-and-true method of protecting seed pieces from disease is
to “cut, treat, and plant”. The less time that elapses between cutting,
treating and planting, the less the risk of disease spread. The risk and degree
of secondary spread increases with the length of time cut seed pieces are held
before treating according to research done in Maine (10). If no seed dressing is
applied at the time of cutting and the seed pieces are held for several days,
the contaminated seed pieces become infected and within days, abundant spores
are produced on their cut surfaces (4). These spores are further dispersed
during handling and planting (10). Such secondarily infected seed pieces are more
likely to survive and produce infected stems than the original infected seed
pieces, which frequently succumb to soft rot.

We studied the efficacy of thiophanate methyl plus mancozeb (Tops MZ) applied at
different times following cutting of seed tubers and inoculation of seed pieces
with P. infestans on stand establishment. Tops MZ protected seed
pieces against P. infestans when applied immediately following cutting
and inoculation (Fig. 8A and B). Emergence approached 100% and seed piece decay
averaged 1.3 and 1.6% in Oregon and Washington, respectively. When the seed
treatment was delayed either 1 or 3 days, Tops MZ was no longer effective in
improving emergence or maintaining seed health (Fig. 9A and B). Across a range
of inoculum densities, percent seed piece decay averaged 90.7 and 92% in Oregon
and 100 and 100% in Washington when the seed treatment was delayed 1.5 or 3.0
days, respectively. This is not unexpected because thiophanate methyl plus mancozeb
has protective, but no curative properties.

Fig. 8. Effect of timing of seed piece treatment on emergence of seed pieces
49 days after inoculation with Phytophthora infestans in (A) Oregon and (B)
Washington. Seed pieces of potato cultivar Shepody were inoculated with sporangia of P.
infestans genotype US-8 in Oregon and US-11 in Washington and then treated
with thiophanate methyl + mancozeb (Tops MZ) immediately, 1.5 or 3 days after
inoculation (click image for larger view).

Fig. 9. Effect of timing of seed piece treatment on seed piece decay 49 days
after inoculation with Phytophthora infestans in (A) Oregon and (B)
Washington. Seed pieces of potato cultivar Shepody were inoculated with sporangia of P.
infestans genotype US-8 in Oregon and US-11 in Washington and then treated
with thiophanate methyl + mancozeb (Tops MZ) immediately, 1.5, or 3 days after
inoculation (click image for larger view).

Challenges and Outlook

Planting of pathogen-free seed is a critical component for management of late
blight. Investigations of seed lots in Germany have shown that up to 20% of the
tubers can be latently infected with P. infestans, even if no symptoms of
tuber blight are evident (1). Therefore, a rapid and accurate method for
specific detection of P. infestans in tubers prior to planting could help
prevent introduction of infected seed pieces into the field. PCR primers have
been developed by researchers at North Carolina State University (16) and at the
USDA-ARS laboratory (15) at Fort Detrick, MD for the specific amplification of P.
infestans in tuber tissue. The need for a rapid, sensitive assay for late
blight in tubers based on more than visual observation or isolation of the
pathogen has been indicated, as some states are considering tightening
tolerances for late blight in seed potatoes.

Until protocols for inspecting and sampling potato seed crops for late blight
are developed, standardized, and accepted by the industry, the number one
relationship that growers may want to cultivate is with the seed producers
themselves. Dealing with reputable seed growers is probably the single best
guarantee because these individuals usually have records of late blight
occurrence in their seed fields. In the meantime the grower should check the
seed tubers for symptoms of late blight prior to receiving delivery. Latent
infections, however, will not be detected visually. Seed from cold storage often
does not exhibit symptoms of late blight but if incubated at 20 to 22°C for 2 to
3 weeks, blight symptoms may develop. This approach allows for proactive
management that targets the seed as the principle source of the inoculum.

Environment is certainly central to the establishment of late blight in the
field. Based on our experiments over the past several years, it is our
hypothesis that soil environmental conditions that favor rapid seed germination
also favor seed transmission of late blight; e.g., planting seed into warm, moist
soils will increase the likelihood of transmission. Our work supports earlier
observations by Hirst and Stedman (5) in England that warm, moist conditions
favor the appearance of stem lesions. Conversely, soil conditions that favor
rapid seed piece decay result in a reduction in stand, but less transmission of
late blight. The disease forecasting system, Blightcast (8), has been used
successfully to predict the appearance of late blight in potato plantings in
central and eastern United States. Little information currently exists
on soil environmental conditions that favor seed transmission, an area ripe for
future investigation.

Seed transmission rates do vary among cultivars. In the Pacific Northwest,
the disease is usually first noted in the cultivars Russet Norkotah and Shepody,
cultivars that are very susceptible to the foliar phase of the disease. In a
study conducted in New York (3) on seed transmission with US-1, late blight
usually, but not always, appeared in the susceptible cultivars before it
appeared in the moderately resistant ones. Transmission frequency appears to be
related more to susceptibility of the foliage than the susceptibility of the
tuber. The release of cultivars with improved resistance to the foliar phase of
the disease may translate into improved resistance to seed transmission.

One of the most cost effective approaches for preventing the spread of the
disease during the seed handling operation is to treat seed pieces immediately
after cutting with a product that has activity against P. infestans. The
value of this approach is twofold: (i) it protects seed pieces from spores that
are spread during the seed handling operation, and (ii) it reduces the number of
spores produced on the cut surface of blighted seed pieces. If application of a
seed dressing is delayed following seed cutting, the opportunity for seed
infection is increased. Products that are currently registered are not effective
against these newly established infections because, for the most part, the
fungicides lack curative activity.

Currently, we are studying the efficacy of applying a fungicide with curative
activity to the foliage at emergence. The objective of this tactic is to target
the first cycle of disease that originates from seedborne inoculum. Because the
appearance of stem lesions usually occurs between 10 and 40 days after planting,
a curative fungicide is banded over the row within the first two weeks after 95%
emergence followed by a second application 10 days to 2 weeks later. The
coupling of a seed piece treatment with a foliar fungicide applied very early in
the season is a two-prong approach for managing late blight that is introduced
into a planting via seed.

Acknowledgements

Research was supported, in part, by grants from the National Potato Council,
the Oregon Potato Commission, the Washington State Potato Commission, Gustafson, Inc,
and Syngenta. Technical paper 11858 of the Oregon Agricultural Experiment Station.